Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms18040844
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dc.titleHypaphorine attenuates lipopolysaccharide-induced endothelial inflammation via regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathway
dc.contributor.authorSun, H
dc.contributor.authorZhu, X
dc.contributor.authorCai, W
dc.contributor.authorQiu, L
dc.date.accessioned2020-11-17T06:33:38Z
dc.date.available2020-11-17T06:33:38Z
dc.date.issued2017
dc.identifier.citationSun, H, Zhu, X, Cai, W, Qiu, L (2017). Hypaphorine attenuates lipopolysaccharide-induced endothelial inflammation via regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathway. International Journal of Molecular Sciences 18 (4) : 844. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms18040844
dc.identifier.issn1661-6596
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/183535
dc.description.abstractEndothelial lesion response to injurious stimuli is a necessary step for initiating inflammatory cascades in blood vessels. Hypaphorine (Hy) from different marine sources is shown to exhibit anti-inflammatory properties. However, the potential roles and possible molecular mechanisms of Hy in endothelial inflammation have yet to be fully clarified. We showed that Hy significantly inhibited the positive effects of lipopolysaccharide (LPS) on pro-inflammatory cytokines expressions, including tumor necrosis factor-α (TNF-α)), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and vascular cellular adhesion molecule-1 (VCAM-1), as well as induction of the phosphorylation of Akt and mTOR in HMEC-1 cells. The downregulated peroxisome proliferator-activated receptor γ (PPAR-γ) and upregulated toll-like receptor 4 (TLR4) expressions in LPS-challenged endothelial cells were prevented by Hy. Inhibition of both PI3K and mTOR reversed LPS-stimulated increases in TLR4 expressions and decreases in PPAR-γ levels. Genetic silencing of TLR4 or PPAR-γ agonist pioglitazone obviously abrogated the levels of pro-inflammatory cytokines in LPS-treated HMEC-1 cells. These results suggest that Hy may exert anti-inflammatory actions through the regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathways. Hy may be considered as a therapeutic agent that can potentially relieve or ameliorate endothelial inflammation-associated diseases. © 2017 by the authors. Licensee MDPI, Basel, Switzerland.
dc.publisherMDPI
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjecthypaphorine
dc.subjectindole alkaloid
dc.subjectinterleukin 1beta
dc.subjectlipopolysaccharide
dc.subjectmonocyte chemotactic protein 1
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein kinase B
dc.subjectrapamycin
dc.subjecttoll like receptor 4
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectvascular cell adhesion molecule 1
dc.subjectautacoid
dc.subjectbiological marker
dc.subjectcytokine
dc.subjectindole derivative
dc.subjectlenticin
dc.subjectlipopolysaccharide
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectphosphatidylinositol 3 kinase
dc.subjectprotein binding
dc.subjectprotein kinase B
dc.subjecttarget of rapamycin kinase
dc.subjecttoll like receptor 4
dc.subjectArticle
dc.subjectcell culture
dc.subjectcontrolled study
dc.subjectdensitometry
dc.subjectenzyme linked immunosorbent assay
dc.subjecthuman
dc.subjecthuman cell
dc.subjectimmunofluorescence microscopy
dc.subjectinflammation
dc.subjectreal time polymerase chain reaction
dc.subjectsignal transduction
dc.subjectstimulation
dc.subjectWestern blotting
dc.subjectdrug effects
dc.subjectenzyme activation
dc.subjectgenetics
dc.subjectinflammation
dc.subjectmetabolism
dc.subjectpathology
dc.subjectsignal transduction
dc.subjectvascular endothelium
dc.subjectBiomarkers
dc.subjectCytokines
dc.subjectEndothelium, Vascular
dc.subjectEnzyme Activation
dc.subjectHumans
dc.subjectIndoles
dc.subjectInflammation
dc.subjectInflammation Mediators
dc.subjectLipopolysaccharides
dc.subjectPhosphatidylinositol 3-Kinases
dc.subjectPPAR gamma
dc.subjectProtein Binding
dc.subjectProto-Oncogene Proteins c-akt
dc.subjectSignal Transduction
dc.subjectToll-Like Receptor 4
dc.subjectTOR Serine-Threonine Kinases
dc.typeArticle
dc.contributor.departmentDEPT OF PHARMACOLOGY
dc.description.doi10.3390/ijms18040844
dc.description.sourcetitleInternational Journal of Molecular Sciences
dc.description.volume18
dc.description.issue4
dc.description.page844
dc.published.statePublished
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